Ca(2+) signalling and PKCalpha activate increased endothelial permeability by disassembly of VE-cadherin junctions

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dc.contributor.authorSandoval, R.en
dc.contributor.authorMalik, A. B.en
dc.contributor.authorMinshall, R. D.en
dc.contributor.authorKouklis, P.en
dc.contributor.authorEllis, C. A.en
dc.contributor.authorTiruppathi, C.en
dc.date.accessioned2015-11-24T19:32:04Z
dc.date.available2015-11-24T19:32:04Z
dc.identifier.issn0022-3751-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/23360
dc.rightsDefault Licence-
dc.subjectAlbumins/pharmacokineticsen
dc.subjectAntigens, CDen
dc.subjectCadherins/*metabolismen
dc.subjectCalcium/metabolismen
dc.subjectCalcium Signaling/drug effects/*physiologyen
dc.subjectCarcinogens/pharmacologyen
dc.subjectCell Membrane Permeability/drug effects/physiologyen
dc.subjectCells, Cultureden
dc.subjectCytoskeletal Proteins/metabolismen
dc.subjectDesmoplakinsen
dc.subjectElectric Impedanceen
dc.subjectEndothelium, Vascular/cytologyen
dc.subjectEnzyme Inhibitors/pharmacologyen
dc.subjectHemostatics/pharmacologyen
dc.subjectHumansen
dc.subjectIntercellular Junctions/*enzymologyen
dc.subjectIodine Radioisotopes/diagnostic useen
dc.subjectIsoenzymes/*metabolismen
dc.subjectMyosin Light Chains/metabolismen
dc.subjectNaphthalenes/pharmacologyen
dc.subjectProtein Kinase C/*metabolismen
dc.subjectProtein Kinase C-alphaen
dc.subjectStress Fibers/physiologyen
dc.subjectTetradecanoylphorbol Acetate/pharmacologyen
dc.subjectThapsigargin/pharmacologyen
dc.subjectThrombin/pharmacologyen
dc.subjectUmbilical Veins/cytologyen
dc.titleCa(2+) signalling and PKCalpha activate increased endothelial permeability by disassembly of VE-cadherin junctionsen
heal.abstract1. The role of intracellular Ca(2+) mobilization in the mechanism of increased endothelial permeability was studied. Human umbilical vein endothelial cells (HUVECs) were exposed to thapsigargin or thrombin at concentrations that resulted in similar increases in intracellular Ca(2+) concentration ([Ca(2+)](i)). The rise in [Ca(2+)](i) in both cases was due to release of Ca(2+) from intracellular stores and influx of extracellular Ca(2+). 2. Both agents decreased endothelial cell monolayer electrical resistance (a measure of endothelial cell shape change) and increased transendothelial (125)I-albumin permeability. Thapsigargin induced activation of PKCalpha and discontinuities in VE-cadherin junctions without formation of actin stress fibres. Thrombin also induced PKCalpha activation and similar alterations in VE-cadherin junctions, but in association with actin stress fibre formation. 3. Thapsigargin failed to promote phosphorylation of the 20 kDa myosin light chain (MLC(20)), whereas thrombin induced MLC(20) phosphorylation consistent with formation of actin stress fibres. 4. Calphostin C pretreatment prevented the disruption of VE-cadherin junctions and the decrease in transendothelial electrical resistance caused by both agents. Thus, the increased [Ca(2+)](i) elicited by thapsigargin and thrombin may activate a calphostin C-sensitive PKC pathway that signals VE-cadherin junctional disassembly and increased endothelial permeability. 5. Results suggest a critical role for Ca(2+) signalling and activation of PKCalpha in mediating the disruption of VE-cadherin junctions, and thereby in the mechanism of increased endothelial permeability.en
heal.accesscampus-
heal.fullTextAvailabilityTRUE-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/11389203-
heal.journalNameJ Physiolen
heal.journalTypepeer-reviewed-
heal.languageen-
heal.publicationDate2001-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.typejournalArticle-
heal.type.elΆρθρο Περιοδικούel
heal.type.enJournal articleen

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